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Synaptopodin-deficient mice lack a spine apparatus and show deficits in synaptic plasticity

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Korte,  M.
Department: Cellular and Systems Neurobiology / Bonhoeffer, MPI of Neurobiology, Max Planck Society;

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Stefani,  G. G.
Department: Cellular and Systems Neurobiology / Bonhoeffer, MPI of Neurobiology, Max Planck Society;

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Bonhoeffer,  T.
Department: Cellular and Systems Neurobiology / Bonhoeffer, MPI of Neurobiology, Max Planck Society;

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Citation

Deller, T., Korte, M., Chabanis, S., Drakew, A., Schwegler, H., Stefani, G. G., et al. (2003). Synaptopodin-deficient mice lack a spine apparatus and show deficits in synaptic plasticity. Proceedings of the National Academy of Sciences of the United States of America, 100(18), 10494-10499.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0012-2305-7
Abstract
The spine apparatus is a cellular organelle that is present in many dendritic spines of excitatory neurons in the mammalian forebrain. Despite its discovery >40 years ago, the function of the spine apparatus is still unknown although calcium buffering functions as well as roles in synaptic plasticity have been proposed. We have recently shown that the 100-kDa protein synaptopodin is associated with the spine apparatus. Here, we now report that mice homozygous for a targeted deletion of the synaptopodin gene completely lack spine apparatuses. Interestingly, this absence of the spine apparatus is accompanied by a reduction in hippocampal long-term potentiation (LTP) in the CA1 region of the hippocampus and by an impairment of spatial learning in the radial arm maze test. This genetic analysis points to a role of the spine apparatus in synaptic plasticity.